BCL11B haploinsufficiency across the major molecular subtypes of T-ALL. Gene expression profiling was previously performed on 40 of the 47 T-ALL cases in the first DFCI/COG cohort, and on all 70 cases in the second cohort of cases from St Jude/COG/AIEOP analyzed in our study, both representing cohorts that are enriched for high-risk ETP/ABD T-ALL cases. Red arrows point to cases with BCL11B mutations or deletions, and black stars mark cases with the ETP phenotype. Samples are classified by T-ALL subtype as follows: ABD, absence of biallelic TCRγ deletion. ETP indicates early T-cell precursor phenotype. HOXA/MEIS, cases with over-expression of genes of the HOXA/MEIS1 cluster, defined as expression values > 100. TLX, cases with TLX1 or TLX3 overexpression. LEF1 (−), cases with LEF1 deletions or truncating mutations.⁴  TAL1, cases with TAL1 expression values > 100 or TAL1 activating deletions. (A-B) Heatmap depiction of gene expression and mutation data from the first cohort of 47 children with T-ALL. (C-D) Heatmap depiction of gene expression and mutation data from the second cohort of 70 children with T-ALL. The expression pattern of selected T-ALL oncogenes in each cohort is shown in panels A and C, based on the expression microarrays applied. Note that probe sets that showed no detectable expression in any sample (defined as expression values < 100) were excluded. Key T-ALL oncogenic alterations in each sample are depicted by green boxes in panels B and D, which represent the presence of NOTCH1 mutations, TAL1 activating deletions, PTEN-PI3K-AKT mutations or PTEN deletions, RAS mutation or NF1 deletion, MYB duplications, FBXW7 mutations or deletions, and CDKN2A deletions (supplemental Table and J.R.D. and C.G.M., manuscript submitted, May 2011).